(1) Background and (2) Methods: A 14-day in vivo, multitoxic (pure mycotoxins) rat experiment was conducted with zearalenone (ZEA; 15 μg/animal/day), deoxynivalenol (DON; 30 μg/animal/day) and fumonisin B1 (FB1; 150 μg/animal/day), as individual mycotoxins, binary (FD, FZ and DZ) and ternary combinations (FDZ), via gavage in 1 mL water boluses. (3) Results: Body weight was unaffected, while liver (ZEA↑ vs. DON) and kidney weight (ZEA↑ vs. FDZ) increased. Hepatocellular membrane lipid fatty acids (FAs) referred to ceramide synthesis disturbance (C20:0, C22:0), and decreased unsaturation (C22:5 n3 and unsat. index), mainly induced by DON and to a lesser extent by ZEA. The DON-FB1 interaction was additive on C20:0 in liver lipids. In renal phospholipids, ZEA had the strongest effect on the FA profile, affecting the saturated (C18:0) and many n6 FAs; ZEA was in an antagonistic relationship with FB1 (C18:0) or DON (C18:2 n6, C20:1 n9). Hepatic oxidative stress was the most expressed in FD (reduced glutathione and glutathione peroxidase), while the nephrotoxic effect was further supported by lipid peroxidation (malondialdehyde) in the DON treatment. (4) Conclusions: In vivo study results refer to multiple mycotoxin interactions on membrane FAs, antioxidants and lipid peroxidation compounds, needing further testing.

Scarce studies have investigated the impact of fumonisin B1 (FB1) on the hepatic tissue fatty acid (FA) profile, and no study is available on piglets. A 10-day in vivo experiment was performed on seven piglets/group: control and FB1-fed animals (diet was contaminated with fungal culture: 20 mg FB1/kg diet). Independent sample t-test was carried out at p < 0.05 as the significance level. Neither growth, nor feed efficiency, was affected. The hepatic phospholipid (PL) fatty acids (FAs) were more susceptible for FB1, while triglyceride (TG) was less responsive. The impact of FB1 on hepatic PL polyunsaturated fatty acids (PUFAs) was more pronounced than on saturated fatty acids. Among all PUFAs, predominant ones in response were docosapentaenoicacid (DPA) (↓), docosahexaenoic DHA (↓) and arachidonic acids (↑). This led to a higher omega-6:omega-3 ratio, whereas a similar finding was noted in TGs. Neither total saturation (SFA) nor total monousaturation (MUFA) were affected by the FB1 administration. The liver showed an increase in malondialdehyde, as well as antioxidant capacity (reduced glutathione and glutathione peroxidase). The plasma enzymatic assessment revealed an increase in alkaline phosphatase (ALP), while alanine transaminase (ALT), aspartate transaminase (AST), lactate dehydrogenase (LDH), and gamma-glutamyltransferase (GGT) were not influenced. The microscopic sections provided evidence of vacuolar degeneration of the hepatocytes’ cytoplasm, but it was not severe. Furthermore, the lung edema was developed, while the kidney was not affected. In conclusion, regarding FB1-mediated hepatotoxicity in piglets, the potential effect of slight hepatotoxicity did not compromise growth performance, at least at the dose and exposure period applied.

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Male Wistar rats were treated intraperitoneally (i.p.) with fumonisin B1 (FB1; 0, 20, 50 and 100 mg/kg dietary dose equivalent) for 5 and 10 days (n = 24–24 in each setting) to gain dose- and time-dependent effects on antioxidant status and oxidative stress response, clinical chemical endpoints and liver, kidney and lung histopathology and lymphocyte damage (genotoxicity). FB1 decreased feed intake, body weight gain and absolute liver weight, irrespective of the toxin dose. Relative kidney weight increased in the 10-day setting. Linear dose response was found for plasma aspartate aminotransferase, alanine aminotransferase, total cholesterol, urea and creatinine, and exposure time-dependence for plasma creatinine level. The latter was coupled with renal histopathological findings, tubular degeneration and necrosis and the detachment of tubular epithelial cells. The pronounced antioxidant response (reduced glutathione accretion, increasing glutathione peroxidase activity) referred to renal cortical response (5–10 days exposure at 50–100 ppm FB1). Hepatic alterations were moderate, referring to initial phase lipid peroxidation (exposure time dependent difference of conjugated diene and triene concentrations), and slight functional disturbance (↑ total cholesterol). Lymphocyte DNA damage was moderate, supporting a mild genotoxic effect of FB1.

At exactly the individual permitted EU-tolerance dietary limits, fumonisins (FB: 5 mg/kg diet) and mixed fusariotoxins (DZ: 0.9 mg deoxynivalenol + 0.1 mg zearalenone/kg diet, and FDZ: 5 mg fumonisins + 0.9 mg deoxynivalenol + 0.1 mg zearalenone/kg diet) were administered to piglets (n = 6/group) for three weeks. Bodyweights of intoxicated piglets increased, while feed conversion ratios decreased. In FDZ, both the absolute and relative weight of the liver decreased. In the renal-cellular membrane, the most pronounced alterations were in FDZ treatment, followed by individual FB exposure. In both treatments, high proportions of C20:0 and C22:0 with low fatty acid (FA) unsaturation were found. In hepatocyte phospholipids, FDZ toxins exerted antagonistic interactions, and FB had the strongest increasing effect on FA monounsaturation. Among all investigated organs, the spleen lipids were the least responsive, in which FDZ expressed synergistic reactions on C20:0 (↑ FDZ vs. FB) and C22:0 (↓ FDZ vs. DZ). The antioxidant defense of the kidney was depleted (↓ glutathione concentration by FB-exposure). Blood plasma indicated renal injury (profound increase of urea and creatinine in FB vs. DZ and FDZ). FB strongly increased total-cholesterol and low density lipoprotein concentrations, whereas FDZ synergistically increased gamma-glutamyltransferase, alkaline-phosphatase, calcium and phosphorus levels. Summarized, individual and combined multiple fusariotoxins modified the membrane lipid profile and antioxidant defense of splanchnic organs, and serum biochemicals, without retarding growth in piglets.